Ch 23 Cancer Genetics Flashcards

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1
Q

what is cancer?

A

a heterogenous group of disorders characterized by the presence of cells that do not respond to normal cell division

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2
Q

what is a tumor?

A

a distinct mass of abnormal cells

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3
Q

what is meant when cancer is benign?

A

tumor cells remain localized

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4
Q

what is meant when cancer is malignant?

A

tumor cells invade other tissues

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5
Q

what is meant when cancer is metastatic?

A

tumor cells travel to other sites where they can establish secondary tumors

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6
Q

how can cancer be nongenetic?

A
  • if cancer is inherited, every cell should have cancer, caused by the cancer causing gene
  • tumors appear only in some tissues
  • tumors often appear when a certain age is reached
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7
Q

what does Knudsen’s proposal suggest about cancer?

A

cancer is a multistep process that requires several mutations

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8
Q

explain the clonal evolution of tumors

A

mutations enhance cells’ ability to proliferate and become the most common cells in a clone, allowing the clone to become increasingly rapid in growth and aggressive in proliferation properties

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9
Q

normal cellular gene responsible for normal cell gunction

A

proto-oncogene

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10
Q

gene that stimulates cell division, leading to tumors forming and cancer

A

oncogene

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11
Q

are oncogenes dominant or recessive acting? why?

A

dominant-acting; the amount of gene product produced by one allele is enough to have a stimulatory effect

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12
Q

genes that normally inhibit cell division

A

tumor-suppressor genes

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13
Q

are tumor-suppressor genes dominant or recessive acting? why?

A

both copies of the allele must be mutated to remove inhibition

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14
Q

inactivation of remaining wild-type allele of a heterozygote

A

loss of heterozygosity

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15
Q

appearance of mutant phenotype in individual that is heterozygous for the trait

A

haploinsuffiency

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16
Q

explain how mutations in (proto)oncogenes can contribute to cancer?

A

a mutation in a proto-oncogene results in an oncogene that stimulates cell division without normal controls, leading to cell proliferation

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17
Q

explain how mutations in tumor-suppressor genes can contribute to cancer?

A

a mutation in a tumor-suppressor gene prevents the gene from inhibiting cell division, leading to excessive cell proliferation

18
Q

what are the roles of CDKs? how are they functional?

A

CDKs add phosphate groups to other proteins, either activating or inactivating the protein
they are functional only when they are associated with cyclin

19
Q

what are the roles of cyclin and how do they contribute to the cell cycle?

A

cyclins associate with CDKs, activating them and making them function. cyclins levels oscillate during the cell cycle, allowing the cell to pass through certain stages

20
Q

describe the G1-S transition
(what checkpoint? what proteins are involved? how does the cell transition into the next stage?)

A

retinoblastoma (RB) protein binds to E2F, inactivating it
as cyclins D & E increase in G1, they associate with CDKs and phosphorylate RB, inactivating it, which releases E2F
E2F goes to transcribe products necessary for DNA replication –> S phase

21
Q

what is the role of the retinoblastoma (RB) protein in the G1-S transition?

A

RB prevents the cell from passing the G1/S checkpoint by binding E2F and inactivating it

22
Q

what would happen if there was a mutation in the RB protein?

A

the RB protein won’t be able to bind and inactivate E2F, therefore cell division is always occurring without normal controls

23
Q

describe the G2-M transition

A

inactive MPF (cyclin-B + CDK) is dephosphorylated, and critical levels of active MPF allow cell to enter mitosis and divide

24
Q

what is the mitosis-promoting factor (MPF) composed of?

A

cyclin-B and CDK

25
Q

what occurs when cyclin-B levels increase in G2

A

increasing cyclin-B concentrations combine with CDKs to form active MPFs, which phosphorylates other proteins that bring about events of mitosis

26
Q

what happens in metaphase, regard cyclin levels?

A

cyclin-B is rapidly degraded in metaphase, which lowers the amount of active MPF, bringing about events that end mitosis

27
Q

what is p53 and what is it regulate?

A

p53 is a tumor-suppressor gene; regulate an inhibitor of CDK

28
Q

what would happen if there was a mutation in the p53 gene?

A

CDK activity would stay constant, causing cell proliferation

29
Q

programmed cell death

A

apoptosis

30
Q

how does apoptosis relate to cancer?

A

cancer cells usually have defects in cellular components that stimulate apoptosis, and cells that need to die proliferate

31
Q

how does autophagy relate to cancer?

A

autophagy allows cancer cells to s

32
Q

explain how the Ras signal transduction pathway is important in the cell cycle

A

external growth factors bind to receptors that allow adapter molecules to bind, which link to an inactive Ras protein. Ras binds GTP, activating, and activates a series of steps, resulting in the activation of transcription factors that transcribe genes of the cell cycle

33
Q

how do mutations in Ras genes contribute to cancer?

A

mutations in Ras genes produce mutant Ras proteins that are always active and continuously stimulate cell division

34
Q

how are DNA-repair genes and mechanisms associated with cancer?

A

defects in DNA-repair genes prevent DNA-repair mechanisms fixing defects in genes that may contribute to cancer

35
Q

explain how mutations in telomerase expression contribute to cancer?

A

mutations in telomerase lead to telomerase being constantly expressed in somatic cells, which allows for unlimited cell division

36
Q

growth of new blood vessels

A

angiogenesis

37
Q

how do mutations in genes that promote vascularization contribute to cancer?

A

tumors need oxygen and nutrients to survive. mutations in genes that promote the growth of new blood vessels allows these tumors to stay and grow

38
Q

why would a reduction in miRNAs contribute to cancer?

A

miRNAs are responsible for degrading or inhibiting the translation of mRNA
reduction in miRNAs may allow oncogenes that are normally suppressed to be highly expressed

39
Q

explain how hypomethylation is associated with cancer

A

lowered DNA methylation leads to transcription of oncogenes that allow for cancer

40
Q

explain how hypermethylation is associated with cancer

A

higher DNA methylation leads to tumor-suppressant genes being inhibited